The aim of this project has been to elucidate the nature of bacteriophages and their role in the mechanisms of genetic exchange (lysogenic conversion, transduction, transformation) and their effect in the pathogenicity and immunogenicity of Group A streptococci. In studies on transduction of the M-protein, a donor strain rich in M-protein was cloned after bactericidal and mouse passages. Further work on erythrogenic toxin strengthens the hypothesis that lysogeny is not essential for the production of ET-B toxin. A "cured" ET-A+, B+ strain lost the ability to synthesize ET-A+ but not ET-B+. Four streptococcal bacteriophages isolated from different serological streptococcal groups showed identical lytic patterns, immunological reactions and transduction patterns. In other collaborative studies we showed that ATFII, the extracellular factor from Pseudomonas fluorescens, controlled T. cruzi infection in mice. After extended treatment the parasites disappeared from the blood stream and normal tissue architecture was restored.